Q and A: Energy-dependent cell type differentiation

By: James V. Kohl | Published on: August 8, 2016

Richard Lenski and other theorists will not discuss the amount of pseudoscientific nonsense they have included in their ridiculous claims. Rarely does anyone else attempt to unravel their claims in the context of the reports I will cite below, or in other reports that refute ridiculous neo-Darwinian theories. Recently, however, Greg Thurston made an honorable effort to learn about energy-dependent biophysically constrained cause and effect via a series of questions that could be answered with minimal jargon.
Q and A from correspondent: Greg Thurston Topic: Energy-dependent changes in the structure of supercoiled DNA
Q1) So this means that no changes would have occurred without energy being available?

A1) The availability of energy is nutrient-dependent and altered by viruses. The lack of any differences in bacteria living in ocean sediments suggests that the absence of sunlight or presence of its biological energy determines all energy-dependent changes in morphological and behavioral phenotypes. Weekend evolution of the bacterial flagellum links virucidal UV light to florescence in P. fluorscens via nutrient-energy uptake and the physiology of pheromone controlled reproduction.

Q2) is there a difference between supercoiled DNA and regular DNA?

A2) Chromatin folding is energy-dependent. The difference in supercoiled DNA compared to any state that is not supercoiled is linked from nutritional epigenetics to the physiology of reproduction, or from virus-driven energy theft to all pathology.

Q3) When you say “from angstroms to ecosystems in all living genera” you mean to say from the smallest observable to the largest observable entities in biology? The whole nine yards, virtually everything?

A3) Yes. The differences in angstroms are not routinely observable, which is why they were not considered in the context of virus-driven pathology — until recently.

Q4) “innate immune system” is there any other type of immune system?

A4) Some people report there is an adaptive immune system, but I don’t know the difference between the innate immune system and an adaptive immune system. The innate immune system enables ecological adaptations, which are manifested in morphological and behavioral phentoypes.

Q5) Do all living genera have an innate immune system?

A5) I’m not sure that any individual or species can survive without one, but  I cannot prove that “all living genera” have an innate immune system.

Q6) When you say “linked energy-dependent changes in the structure … via the innate immune system and the physiology of reproduction.” Do you mean changes in the structure were linked TO the innate immune system and the physiology of reproduction, or TO SOMETHING ELSE via these two things?

A6) Energy-dependent changes must be linked from the innate immune system to the physiology of reproduction for fixation of RNA-mediated amino acid substitutions to occur in the organized genomes of specific populations.

Q7) If the latter, what is the ‘something else’?

A7) No one has made claims that fixation occurs outside the context of the physiology of reproduction except those who put fixation of beneficial mutations into the context of population genetics. Pseudoscientists do that because otherwise neo-Darwinian theory has no explanatory power. The neo-Darwinists won’t tell you what was selected. And, they don’t mention virus-driven energy theft. Some are changing their claims about natural selection, but most still claim that mutations are selected. Without their ridiculous claims they have no theory, so they continue to claim that something must have been selected.

Q8)”Supercoiled DNA protects all organized genomes” — are there any genomes which are not organized?

A8) Incompletely organized genomes are found in behavioral morphs of some species that have not yet diverged (e.g., white throated sparrows)

Q9) “from virus-driven entropy.”  what other kind of entropy is there, and what drives it?

A9) I use “entropy” in the context of thermodynamic cycles of protein biosynthesis and degradation. That helps to avoid debate about theories about open or closed systems.

Q10) Is there anything else which supercoiled DNA protects genomes from, or is it all virus-driven?

A10) I’m not willing to speculate. I’m providing facts linked to biologically-based cause and effect.

Q11) “The virucidal effect of ultraviolet light on RNA-mediated cell type differentiation is the source of all biodiversity. ” — Virucidal means UV light kills viruses?

A11) Yes.

Q12) Is there any other type besides RNA-mediated cell type differentiation?

A12) Not to my knowledge.

Q13) Are you saying that all biodiversity would not occur unless UV light was virucidal?

A13) I’m saying that mutation-driven evolution is not supported with experimental evidence of biologically-based cause and effect.

Q14) “the source of all biodiversity is biophysically constrained” — in other words there are rules in place which guide everything when it works properly?

A14) Yes. There are Laws of Biology. Biophysically constrained energy-dependent protein folding chemistry guides hydrogen-atom transfer in DNA base pairs in solution, and links microRNA flanking sequences to RNA-mediated amino acid substitutions and all biodiversity.

Q15) “they know that virus-driven energy theft breaks those constraints” — is ‘vdet’ the only thing which breaks those constraints?

A15) To my knowledge, no one else has made claims about how the constraints are broken.

Q16) This gets to the nub of the significance of this. That, I think is the pot of gold. What is the significance that they know, but are keeping mum on it? Is it because if they let the cat out of the bag, Darwinism is dead supposedly?

A16) Yes. But also, all theorists will look foolish for touting neo-Darwinian nonsense. George Church and others may only be protecting their biologically uninformed colleagues in academia.

Q17) Are they holding back science by not broadcasting this?

A17) Yes. The November, 2016 meeting of the Royal Society is scheduled in an attempt to save the theory of evolution via careful extraction of neo-Darwinian nonsense, albeit without claims about virus-driven entropy.

Q18. If they were to broadcast it, how would that change how science is done? (Apart from so many being crestfallen that their god is dead?)

A18) The change from gene-centric neo-Darwinian views to focus on energy-dependent changes in RNA methylation and RNA-mediated amino acid substitutions is required if science is to be done. It does little good to ridicule theorists, however, no matter how much fun it might be to show their god (of mutation-driven evolution) is dead. The ridicule simply encourages them to tell more lies.

Q19) I think I get your last paragraph. Except I’m not sure how methylation fits in there.
A19) RNA-methylation is the energy-dependent link to learning and memory in all living genera.
Thanks again. Your questions will help some others move forward despite the complexity. Ultimately, however, all serious scientists will learn why George Church et al., filed the patent for RNA-guided human genome engineering.
Perhaps they deserve to deliver their “billion dollar baby” without considering others who have placed their “baby” into the context of what was known about RNA-mediated links from fertilization to adult sexual behavior via cell type differentiation for more than 20 years.
But see: C2c2 is a single-component programmable RNA-guided RNA-targeting CRISPR effector
Abstract conclusion:

C2c2 could protect bacteria from virus spread via programmed cell death and dormancy induction. A single-effector RNA targeting system has the potential to serve as a general chassis for molecular tools for visualizing, degrading, or binding RNA in a programmable, multiplexed fashion.

Article excerpt:

…there is a possibility that C2c2 functions solely as an RNA-guided RNA-targeting CRISPR effector.

From their Conclusions:

C2c2 cleaves RNA through conserved basic residues within its two HEPN domains, in contrast to the catalytic mechanisms of other known RNases found in CRISPR-Cas systems (25, 48). Alanine substitution of any of the four predicted HEPN domain catalytic residues converted C2c2 into an inactive programmable RNA-binding protein (dC2c2, analogous to dCas9).


The CRISPR-C2c2 system represent a distinct evolutionary path among class 2 CRISPR-Cas systems. It is likely that other, broadly analogous class 2 RNA-targeting immune systems exist, and further characterization of the diverse members of class 2 systems will provide a deeper understanding of bacterial immunity and provide a rich starting point for the development of programmable molecular tools for in vivo RNA manipulation.

My comment: They link the nutrient energy-dependent pheromone-controlled physiology of reproduction to fixation of the alanine substitution and stability of all organized genomes in the context of other RNA-mediated amino acid substitutions such as Val66Met in mice and Val158Met in humans during life history transitions in morphological and behavioral phenotypes.
See for other examples: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).

These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.

See also: The Genetic Contribution of West-African Ancestry to Protection against Central Obesity in African-American Men but Not Women: Results from the ARIC and MESA Studies


This study suggests that there are specific genetic variants and physiological mechanism(s) that differ among West African and European populations, which when in the context of male sex, result in lower central adiposity. Further research, likely requiring larger sample sizes, is needed to identify these putative specific genetic factors and their corresponding physiological mechanisms. The identification and understanding of these mechanisms could lead to improved prevention and treatment approaches. It will also be important to also consider and examine non-genetic factors that may underlie the greater racial disparity among women.

My comment: Their conclusion ignores everything known to serious scientists about energy-dependent RNA-mediated cell type differentiation which links all sex differences in cell types to all other RNA-mediated differences via the nutrient-dependent pheromone-controlled physiology of reproduction in yeasts and fixation of amino acid substitutions in organized genomes. See: From Fertilization to Adult Sexual Behavior for details on the molecular epigenetics of energy-dependent cell type differention, which have since been linked from one-carbon metabolism to genetic networks in all living genera.

See also: Rapid adaptation of harmful cyanobacteria to rising CO2

Abstract introduction:

Rising atmospheric CO2 concentrations are likely to affect many ecosystems worldwide.

Article conclusion:

In conclusion, our study shows that changes in Ci availability act as an important selective factor in cyanobacterial communities. Some strains perform better at low Ci concentrations, whereas other strains are better competitors at high Ci levels, causing a succession of different Ci uptake genotypes during bloom development. Models and laboratory experiments predict that rising atmospheric CO2 levels will lead to higher CO2(aq) and bicarbonate concentrations, and a later onset and shorter duration of CO2-depleted conditions during dense summer blooms (14, 15). Our results suggest that this increased Ci availability will favor low-affinity but high-flux bicarbonate uptake genotypes. Hence, future harmful cyanobacterial blooms will most likely have a genotype composition that differs from contemporary blooms and will be adapted to the new conditions in a high-CO2 world.

My comment: The harmful blooms link virus-driven energy theft from the proliferation of strains that reproduce faster (‘perform better’) at high Carbon ion concentrations, which link virus-caused changes in hydrogen-atom transfer in DNA base pairs in solution to all pathology in all living genera.

See for comparison: Tempo and mode of genome evolution in a 50,000-generation experiment

Excerpt (with my emphasis):

 One line of evidence derives from the expectation that synonymous substitutionspoint mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate20,35. This expectation is not strictly true owing to selection on codon usage, RNA folding, and other effects, but it is generally thought that such selection is extremely weak, affects only a small fraction of sites at risk for synonymous mutations, or both 36,37.

My comment: They admit that their lie about synonymous substitutions, which they call point mutations, does not hold up to scrutiny in the context of biophysically constrained nutrient energy-dependent RNA-mediated protein folding chemistry. They, they continue to make vague claims about how selection for synonymous mutations occurs. The fact that selection for amino acid substitutions is controlled by the physiology of reproduction in all genera is not given any consideration whatsoever.  It is dismissed with claims about synonymous mutations that were first called synonymous substitutions. They use wordplay to obfuscate the fact that energy-dependent amino acid substitutions are not mutations. Without the wordplay, they would be forces to admit that their experiment is designed to link ecological variation to ecological adaptation via the energy-dependent physiology of pheromone-controlled reproduction in species from microbes to humans.
See for instance two of the works they cited:

Different Trajectories of Parallel Evolution During Viral Adaptation (1999)
Whole genome, whole population sequencing reveals that loss of signaling networks is the major adaptive strategy in a constant environment (2013)
My comment: Lenski’s group clearly knows his experiment links ecological variation to ecological adaptation in a constant evironment. But Lenski has been reporting it as if it linked mutations to evolution.  See: The Man Who Bottled Evolution
See for comparison: Changing Folding and Binding Stability in a Viral Coat Protein: A Comparison between Substitutions Accessible through Mutation and Those Fixed by Natural Selection (2014)

…adaptation may not just be in response to direct selective forces; it may also be influenced circuitously by conditions like temperature and acidity that may select for changes in stability.

My comment: The selective forces link biophysically constrained energy-dependent changes in cell type differentiation to healthy longevity or they link virus-driven energy theft to all pathology. Nothing links the selective forces to the evolution of one species from another. The Man Who Bottled Evolution is the man who bottled long term ecological adaptation in an experiment he referred to as the Long Term Evolution Experiment (LTEE).  Now that Lenski admits he has been caught in a lie, he refuses to move forward by linking codon usage to biophysically constrained RNA-mediated protein folding chemistry, which links the innate immune system to supercoiled DNA without any neo-Darwinian nonsense.
See also:  New Perspectives on Ebola Virus Evolution (2016) with my emphasis

Abstract excerpt: We tested for positive selection and considered the placement of adaptive amino acid substitutions along the phylogeny and within the protein structure of GP1,2. We conclude that: 1) the common practice of rooting the phylogeny of EBOV between the first known outbreak in 1976 and the next outbreak in 1995 provides a misleading view of EBOV evolution that ignores the fact that there is a non-human EBOV host between outbreaks; 2) the N-terminus of GP1 may be constrained from evolving in response to the host immune system by the highly expressed, secreted glycoprotein, which is encoded by the same region of the GP gene; 3) although the mucin-like domain of GP1 is essential for EBOV in vivo, it evolves rapidly without losing its twin functions: providing O-linked glycosylation sites and a flexible surface.

My comment: Positive selection for nutrient energy-dependent RNA-mediated amino acid substitutions again replaces the vague claims about ‘natural’ selection made by neo-Darwinian theorists. The energy-dependent physiology of pheromone-controlled reproduction in mosquitoes must be linked to virus-driven energy theft and DNA damage in humans, or all claims about ‘natural’ selection and evolution must be ignored.
What’s worse is that this admission must also be ignored.

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

My comment: Anyone who claims that any species evolved from another via natural selection in the context of mutation-driven evolution is propagating Lenski’s lie. They must ignore the fact that the physiology of reproduction is energy-dependent and controlled by pheromones in species from microbes to humans.
See for comparison: Epigenetics and Genetics of Viral Latency

… viral latency is responsible for life-long pathogenesis and mortality risk…

1) Ignoring the fact that healthy longevity is nutrient energy-dependent;

2) Ignoring the facts about viral latency, which is linked to all pathology; and

3) Ignoring the fact that a single amino acid substitution in the influenza virus is linked to seasonal differences in its virulence/pathology;

sums up the amount of ignorance that is taught when neo-Darwian theory is taught to unsuspecting students.

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